Pruritus in the Elderly

Clinical Approaches to the Improvement of Quality of Life

Kenneth R. Cohen, PharmD, PhD; Jerry Frank, MD;
Rebecca L. Salbu, PharmD, CGP; and Igor Israel, MD

INTRODUCTION
Case Report
J. D., an 85-year-old female resident of a long-term-care
facility, was recently evaluated for generalized pruritus. Her
medical history includes dementia, diabetes mellitus,
peripheral vascular disease, hypertension, congestive heart
failure, chronic obstructive pulmonary disease,
osteoarthritis, gastroesophageal reflux disease, and a
recurrent urinary tract infection.
Over the clinical course of her disorders, she was taking
multiple medications off and on, including acetaminophen,
fluticasone/salmeterol inhaler, albuterol inhaler, ipratropium
inhaler, docusate sodium, ferrous sulfate, flunisolide nasal
spray, furosemide, lovastatin, insulin, omeprazole, and
enalapril.
These medications were discontinued to determine
whether they were the cause of the patients pruritus. The
discontinuations had no effect on her condition.
Systemic hydroxyzine, diphenhydramine, and prednisone; oral amitriptyline; and topical betamethasone diproprionate ointment were used to treat her pruritic symptoms.
A review of the patients organ systems proved unremarkable. On physical examination, she was noted to be in no
distress. Her cognition was unchanged from her admission
status of mild disorientation, which was consistent with her
dementia.
The remainder of her examination was significant only for
mild excoriations on her stomach and extremities and an
erythematous rash across her buttocks.
Laboratory assessments were within normal values
except for a white blood cell (WBC) count of 11,500 mcL
with a normal differential; a random blood glucose level of
278 mg/dL; and a blood urea nitrogen (BUN) of 42 mg/dL.
The patients pruritus has remained moderately symptomatic; only occasional relief was achieved with medications.
The cause was never determined. The purpose of the
review was to present the possible causes of the pruritus to
assist clinicians in individualizing treatment.

Dr. Cohen is an Associate Professor of Pharmacy and Health Outcomes at the Touro College of Pharmacy in New York, N.Y.
Dr. Frank is a Clinical Assistant Professor in the Department of
Family Medicine at SUNY Stony Brook School of Medicine in Stony
Brook, N.Y. Dr. Salbu is an Assistant Professor of Pharmacy and
Health Outcomes at the Touro College of Pharmacy. Dr. Israel is
Associate Medical Director at the Parker Jewish Institute of Health
Care and Rehabilitation in New Hyde Park, N.Y.

Accepted for publication November 18, 2011.

Pruritus is the most common skin disorder in the geriatric

population.1 It is defined as an unpleasant cutaneous sensation
that provokes the desire to scratch.2 Acute itch (lasting less
than 6 weeks) may provide a protective function, but chronic
itch (lasting more than 6 weeks) is mostly a nuisance.3 The
prevalence of pruritus increases with age and can be partially
attributed to a decline in the normal physiological status of the
skin (Table 1).2,4
In a French study, a survey was sent to 10,000 randomly
selected households.5 Of 7,500 respondents, 87% reported skin
problems since birth and 43% experienced these problems
over the 2 years preceding the survey. In addition, 29% of the
respondents described their symptoms as burdensome. Of
those individuals, more than half indicated that chronic skin
disorders, with pruritus as the primary symptom, impaired
daily activities.
Moreover, in a study of skin disorders in 68 noninstitutionalized persons, two-thirds of the group and 83% of octogenarians reported medical concerns regarding their skin,
with pruritus the most frequent complaint.6 In a study conducted in Norway, itching was the predominant skin complaint in subjects ranging from 30 to 76 years of age.7
Chronic pruritus can have a significant effect on quality of
life, because therapies for acute pruritus often do not ameliorate chronic disease.8 In many people, itching is not just an
occasional problem; it can have debilitating effects, such as
sleep impairment, that can result in clinical depression. In
fact, many people with chronic itching can become so depressed that they would rather live a shorter life free of
symptoms than a longer life with pruritus.8 Studies have shown
Table 1 Decline of Skin Function in the Geriatric
Population

Cell replacement
Barrier function
Chemical clearance capacity
Sensory perception
Mechanical protection
Wound healing
Immune responsiveness
Thermoregulation
Sweat production
Vitamin D production

Data from Tycross R, et al. Q J Med 2003;96:726;2 and Fenske NA,

Lober CW. Geriatrics 1990;45:2735.4

Disclosure: The authors report that they have no financial or commercial/industrial relationships in regard to this article.

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Pruritus in the Elderly

that the detrimental effect of chronic pruritus on quality of life
is comparable with that of chronic pain.8,9

INCIDENCE AND PREVALENCE

As noted, chronic pruritus is one of the most common dermatological complaints of patients, especially in the elderly.
In the study by Beauregard and Gilchrest,6 two-thirds of geriatric patients reported pruritus as their major skin complaint.
The condition is more prevalent in women than in men.7,10
In an analysis of hospital-based patient registry records,
11.5% of hospital admissions in elderly patients were attributed
primarily to pruritus.1 In patients older than 85 years of age,
this incidence rose to nearly 20%. In another study, pruritus was
present in two-thirds of approximately 1,500 elderly patients in
skilled-nursing facilities.11

PATHOPHYSIOLOGY
The sensation of itching is closely associated with the sensations of touch and pain.12 Pruritus is stimulated by the release
of neurostimulators, such as histamine, from mast cells and
other peptides. The resulting sensation of itch is carried on
A-delta and C fibers, through the dorsal horn of the spinal cord,
and across the anterior commissure to the spinothalamic tract,
ultimately terminating in various brain centers, including the
cortex and thalamus.10,1214
Aging skin is susceptible to pruritic disorders because of the
cumulative effects that the environment has on the skin and
because of changes to the skin structure that occur as we
age.15 Loss of skin hydration, loss of collagen, impaired
immune system responses, and impaired function of the skin
as a barrier to pathogens are also involved. Impaired blood
circulation, leading to decreased perfusion to the skin, may also
occur.3 The presence of comorbid conditions, the lack of
mobility, and the increased use of medications may also
contribute to the prevalence of pruritus in elderly individuals.16
In older people, pruritus is often associated with dry skin resulting from decreased skin-surface lipids, reduced production
of sweat and sebum, and decreased perfusion.17 Collagen is
also reduced and is less soluble in geriatric populations. Moreover, because of skin folding, less surface area is able to interact
with water.18 This can result in impaired immune function and
diminished barrier repair. Altered skin pigmentation and
increased skin fragility also increase the likelihood of pruritus
in elderly adults.18

NEUROTRANSMITTERS
The release of histamine from mast cells is believed to be the
primary mediator of itching.19 This release may also cause a
vascular response that results in erythema and swelling of
the affected skin. However, because not all patients with pruritus respond to antihistamine therapy, other mediators appear
to be involved as well.19 For example, serotonin (5-HT) is
released when platelets aggregate and stimulate serotonin
receptors. 5-HT3 antagonists have been shown to reduce
itching.20
Acetylcholine, a neurotransmitter, is also involved in pruritus, particularly in patients with atopic dermatitis.21 These
patients have dry, thickened skin and an increased sensitivity
to acetylcholine.

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Prostaglandins (lipid compounds produced in cells by the

enzyme cyclooxygenase) are involved in the chemical cascade
created by histamine and may potentiate pruritic symptoms
caused by histamine and possibly other agents.22
Nerve fibers containing substance P, a neuropeptide, congregate around sweat glands and blood vessels and can lead
to neurogenic inflammation.23 In addition, vasoactive intestinal peptide (VIP) can produce itching.23 High levels of substance P, VIP, somatostatin, and neuropeptide Y occur in
pruritic skin lesions.23,24 In addition to histamine, activated
mast cells release chymase, tryptase, leukotrienes, and interleukins, which can lead to pruritus.23

CLASSIFICATION AND ETIOLOGY

The classification of pruritus begins with the disorders
etiology.13 The origin can be both dermal and neuropathic.
Pruritus can also originate centrally, or the cause can be
psychogenic.2

Dermatological Causes
The most common dermatological change that occurs in
elderly people is xerosis, or dry skin.25 Environmental conditions or excessive loss of moisture from the epidermis may
result in xerotic lesions, which can crack and split. This in turn
can cause pruritus and bleeding, possibly leading to infection.
Other causes of dry skin include weather extremes, such as
cold air or low humidity, and excessive exposure to water,
especially in colder climates.2527
Excessive exposure to the sun can also lead to a variety of
skin irritations, including sunburn, or it can exacerbate further
drying of xerotic skin lesions.26,27
Scabies, an extremely pruritic skin disorder, commonly
occurs in the elderly, especially those confined to long-termcare facilities.28 Scabies results from infection by the hostspecific mite Sarcoptes scabiei var hominis. Each year, more
than 300 million cases of scabies occur worldwide, and the
infection is highly contagious in institutional settings.28 The
disorder is diagnosed by microscopic examination of skin
scrapings under mineral oil.29
Atopic dermatitis, or eczema, is a recurring inflammatory
skin condition that is often associated with allergic disorders,
such as asthma and allergic rhinitis.30 Exposure to an allergen provokes the release of histamine, which can result in pruritus.
Pruritus is also associated with contact dermatitis. Detergents used in institutional bedding and clothing, as well as the
materials used in the manufacturing of these garments, have
been implicated. Other irritants include fiberglass and environmental cleaning agents.
Infection (e.g., tinea, candidiasis, and herpesvirus) is another
important cause of pruritus. Patients with certain viral infections, such as measles or rubella, commonly experience
intense itching.
Bacterial infections can also cause pruritus; this usually
occurs after scratching has damaged the skin, which allows
bacteria to colonize the affected area. Fecal bacteria may be
transferred to the skin from contaminated hands, or dermal
bacteria, such as streptococci or staphylococci, may grow in
open wounds.29

Pruritus in the Elderly

Neuropathic and Neurogenic Causes
Damage to nerve fibers or to the brain can lead to a particular form of pruritus known as itch without rash.31 This type
of neuropathic itching is processed in the thalamus after the
stimulation of dorsal horn neurons. The itching can be caused
by a variety of nerve-related disorders, including multiple sclerosis and brain tumors.31
After a stroke, damage to the central nervous system (CNS)
can lead to neurogenic pruritus.32,33 In these cases, the sensation of intense itching arises from lesions in the thalamus or
parietal lobe without localized skin irritation.
Pruritus has also been associated with neuralgia following
a herpes infection.34

Psychiatric Causes
Pruritus can result from a number of psychiatric disorders.
In one study, 70% of patients with chronic pruritus had at least
one of six psychiatric diagnoses, including dementia, schizophrenia, primary depressive disorders, personality disorders,
and behavioral disorders.35
The French Psychodermatology Group proposed three compulsory criteria for a diagnosis of psychogenic pruritus:36
localized or generalized itch without skin lesions
chronic itch (lasting more than 6 weeks)
absence of a somatic cause
In addition, at least three of the following seven criteria
should be present:
a chronological relationship with an event that could have
psychological repercussions
stress-related variations in the intensity of the itching
nocturnal variations in symptoms
predominance of the itching during rest or inaction
presence of a psychological disorder associated with itching
itching that can be improved with psychotropic drugs or
psychotherapy

bile salts or of endogenous opioids have been implicated as

well.40 Other causes of neurogenic itch associated with cholestasis include the release of intrinsic opioids or the extrinsic
administration of opiate drugs.41 The symptoms of cholestatic
pruritus are usually more pronounced at night.
Pruritus occurs in up to 90% of patients with renal failure or
uremia who are receiving maintenance dialysis.42 The most
common cause is xerosis secondary to dialysis, which affects
the balance of calcium, magnesium, and phosphorus. In addition, the patients uremic condition acts as a chronic inflammatory process, causing the releasing of proinflammatory
cytokines and histamine.43 Itching does not occur in patients
with acute renal failure.44
The presence of pruritus is one of the four diagnostic hallmarks of diabetes mellitus (i.e., polyuria, polydipsia, polyphagia, and pruritus), although early studies found that itching was
present in only 7% of patients with diabetes.42 The cause of the
intense itching experienced by diabetic patients is unclear,
but it may be related to secondary conditions, such as xerosis
or infections.45 Interestingly, the control of elevated blood
glucose levels often leads to a marked reduction in symptoms.
Several case studies have identified generalized pruritus as
a symptom of thyroid disease. In these patients, the most common cause of pruritus was the presence of antithyroid antibodies.46 Pruritus in patients with hyperthyroidism may be
caused by the warm, moist skin that accompanies this disorder,
although the exact cause is unknown.47 Hyperthyroidism can
also cause cholestatic jaundice, which has been associated
with pruritus.48 In patients with hypothyroidism, pruritus is
usually the result of xerosis.47,49 Treatment of the underlying
condition usually results in the resolution of pruritic symptoms
in patients with thyroid disease.38,47,49
Hematological disorders can also cause pruritus.47 For example, the onset of Hodgkins disease is often preceded by an
intense, burning itch.50 Moreover, generalized pruritus occurs
in 25% to 50% of patients with polycythemia vera (a bone marrow disease associated with an abnormal increase in the number of blood cells).51 Adult-onset eczema has been identified as
a marker for leukemia.50

Pruritus Associated With Systemic Diseases

Drug-Induced Pruritus

Systemic diseases often lower the itch threshold. In this

setting, a mild stimulus can trigger an exaggerated pruritic
response in some patients. Comorbid xerosis resulting from
decreased skin hydration may exacerbate pruritus in older
patients with systemic diseases. This is especially true for
institutionalized geriatric patients or for individuals with dementia whose general inactivity allows them to be distracted
by pruritic stimuli.37
Patients with liver disease often experience pruritus.3840
Itching is a presenting symptom in 25% of those with jaundice
from biliary obstruction or other causes, such as cirrhosis, pancreatic cancer, or hepatitis. 38 It has been hypothesized that
pruritus in these patients might be the result of an accumulation of bile in nerves or skin cells, but this remains unproven.38
Increased levels of plasma lysophosphatidic acid (LPA) and
of serum autotoxin have been obser ved in patients with
cholestatic pruritus.39 Autotoxin is involved in the conversion
of lysophosphatidylcholine to LPA. High concentrations of

Drug-induced pruritus typically results from an allergic

reaction to an active medication or to the fillers or preservatives used in the drugs preparation.52 Drugs can also cause
pruritus indirectly by affecting the liver or kidneys, which
leads to itching owing to liver failure and jaundice or to renal
failure with uremia.52 Some medications, such as angiotensinreceptor blockers (ARBs) and angiotensin-converting enzyme
(ACE) inhibitors, mediate the release of bradykinins, resulting
in pruritus.52
Pruritus may occur as a secondary response to systemic side
effects involving the liver or kidney after treatment with amiodarone (Cordarone, Wyeth/Pfizer), ticlopidine (Ticlid, Roche),
some antibiotics (e.g., macrolides and carbapenems), and
psychotropic agents (e.g., tricyclic antidepressants and
neuroleptics).53,54 Statins (HMGCoA reductase inhibitors),
antimicrobials, chemotherapeutic agents, and antiseizure medications, such as phenytoin (Dilantin, Pfizer), carbamazepine
(Tegretol, Novartis), and topiramate (Topamax, Janssen), may

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cause a rash or skin lesions, with resulting pruritus.5456
Opioids can cause pruritus, most likely as an adverse effect
rather than as an allergic reaction. Pruritus occurs in 2% to 10%
of patients who have been treated with opioids; the mechanism
is thought to be related to the release of histamines or to a
centrally mediated process.57
Some drug reactions that result in pruritus can be severe
and potentially life-threatening. The appearance of acute
urticaria and angioedema, for example, should be considered
a medical emergency, requiring the immediate discontinuation
of the offending agent, followed by treatment with parenteral
antihistamines and prednisone.58
Toxic epidermal necrolysis (TEN), also known as Lyells
syndrome, is one of the most serious drug-related skin
reactions. It involves the initial development of erythema, followed by large vesicles and mucosal erosions. The exposure
of underlying tissue, with fluid loss, can lead to systemic infection and, potentially, fatal septic shock. Phenytoin, barbiturates, penicillin, and sulfonamides are known to cause TEN.58

EVALUATION
Although it can be difficult to identify the cause of pruritus,
therapy is a fairly straightforward process after the origin has
been determined. Treatment consists mainly of removing or
avoiding the offending agent or allergen in conjunction with the
use of topical or systemic drugs.

Medical History
A detailed medical history should be obtained if the primary cause of the patients pruritus is to be identified. The following factors must be considered: 59
1. Initiation of symptoms. Understanding when the pruritus started and its relationship to the introduction of a new
environmental factor, detergent, soap, or food is important. It
should also be determined whether the itching is generalized
or localized, and its location should be pinpointed; this information may point to a primary cause of the disorder. For example, an itch that is localized to the groin or to the anal area
may have a specific cause, such as a fungal or parasitic infection, or it may be secondary to another disorder, such as hemorrhoids.
2. Presence or absence of lesions. The presence or absence of a lesion can help point to the cause. For example, a
pruritic rash that waxes and wanes may indicate an allergic
reaction.
3. Time of day when symptoms are worst. Knowing
when symptoms are most severe may guide the diagnosis toward a primary cause, such as mites or other parasites, which
tend to be more active at night. Pruritus that is worse at bedtime could also be related to irritation from bedding.
4. Identifying what makes the condition better. Some
circumstances may improve the condition, such as immersing
the affected area in cold water or avoiding certain clothes or
soaps.
When seeking a secondary cause, the clinician must consider the presence of other disorders. For example:60

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Polyuria, polydipsia, and polyphagia may indicate the

presence of diabetes mellitus.
A history of anxiety, palpitations, or hair loss may indicate
that the pruritus is associated with hyperthyroidism.
A pruritic patient who is chronically fatigued may have
concomitant hypothyroidism.
Generalized pruritus accompanied by dark brown urine,
abdominal pain and bloating, and yellowing of the skin and
eyes may point to a hepatic origin.
Pruritus accompanied by weight loss may signify an occult neoplasm.61
The presence of diabetes mellitus, liver disease, a thyroid
imbalance, or neoplasia may indicate that the pruritus is
a secondary condition.62
Other important aspects of the patients medical history
include:63,64
Surgery. Determining whether the patient has had surgery for a chronic biliary disorder or has had cancerous
tissue removed can help pinpoint a secondary cause of the
itching.
Medications. Drugs can be a primary cause of chronic
pruritus, and a detailed history of their intake must be
obtained. Noting a relationship between the start of drug
treatment and the beginning of itching could be the key
to identifying its cause. Conversely, a history of improvement after the withdrawal of a drug is also significant.
Allergies. Understanding medication allergies and crosssensitivities is helpful. Well-known cross-sensitivities,
such as penicillin and cephalosporin, can be quickly resolved. Lesser-known cross-reactions should be investigated, especially if the timing of the beginning of the itching coincides with the introduction of a new drug. The
clinician should also investigate the patients use of overthe-counter medications and the cross-reactivity of those
drugs with prescribed agents.
Social history. A history of social behaviors, including
the use of illicit drugs and alcohol, can also assist the
clinician. The recreational use of illicit drugs, such as
opiates, amphetamines, and cocaine, may indicate that a
generalized pruritus is secondary to this behavior.
Family history. A family history of medical conditions
associated with secondary pruritus is important. The occurrence of diabetes mellitus, thyroid disease, or liver disease in other family members may assist the clinician in
reaching a diagnosis.63
Review of systems. A review of the patients organ systems, besides the skin, is an important part of the medical
histor y, as accompanying complaints may guide the
clinician toward a diagnosis of secondary pruritus. Symptoms associated with other organ systems should be
considered, and a further workup should be performed
to exclude specific conditions, based on findings from
the initial review. 64

Physical Examination
The physical examination of a patient with pruritus should
start with a general evaluation.

Pruritus in the Elderly

Vital signs must be assessed. The presence of fever (i.e., a
temperature of more than 100.8oF) may indicate that the pruritus has been caused by an infectious process.
Assessment of the skin, of course, is the most important part
of the physical examination.65 The clinician must check the
skins coloration. The presence or absence of erythema in the
areas affected by the itching can help in diagnosis, especially
infection. Hemorrhage may signify a secondar y cause of
pruritus, such as neoplastic disease. Jaundice may indicate
itching related to liver disease.
During the skin examination, the clinician must also look for
lesions. Pruritic vesicles on the skin are a hallmark of viral infections, such as varicella (chickenpox). Larger lesions (bullae) could be the result of bacterial infections, such as impetigo, or autoimmune disorders. Excoriations in the affected
areas signify the intensity of the itching as well as the possibility of secondary infection, because the barrier properties of
the skin might have been jeopardized. Scaling and cracks in
the skin are hallmarks of xerosis. Localized, itchy macules or
papules may indicate an atopic reaction to an allergen.59
A simple touch of the skin to assess the warmth of the
affected area helps in identifying an infection. The clinician may
palpate the skin for fluctuance when an abscess is suspected
of causing pain and itching. Subcutaneous or subepidermal
lesions should be assessed to determine the need for a biopsy.
The clinician should also examine the skin for tissue turgor
to assess general hydration. In elderly patients, the elasticity
of the skin tends to be lost, so the tenting that is typically seen
in patients with low turgor may be the result of aging, not
dehydration, in these individuals.63
Checking for dermatographism is an easy test to perform.
The clinician strokes the patients skin using the dull side of
an object in a linear motion. If the line remains elevated and
erythematous, the result is considered positive. A positive test
indicates that the patient has overly sensitive skin and that histamines have been released in response to the mild trauma.
This finding usually indicates that an antihistamine should be
prescribed.
Thickening of the skin in a pruritic area can indicate the presence of chronic inflammation, which can result from continuous scratching or irritation.66

Laboratory Tests
Laboratory assessments may be helpful in identifying the
cause of pruritus, but they usually play a supportive role in the
physical examination. The complete blood count might show an
increased white blood cell (WBC) count. A high neutrophil
count, with a large number of immature neutrophils (left shift),
would indicate the presence of a bacterial infection. An elevated
WBC count showing an increased number of eosinophils may
indicate an allergic reaction or the presence of a parasitic infection. A high lymphocyte count, by contrast, may indicate a
viral infection. The presence of any abnormal WBC counts, as
well as the presence of abnormal WBCs, should be reviewed
and considered in terms of a neoplastic process.67
Chemistry panels may indicate the presence of a secondary
cause of the itching. Elevated bilirubin levels confirm an
observation of jaundice, and elevated alkaline phosphatase
levels would pinpoint the cause of the jaundice. Elevated

glucose levels might point to diabetes as a cause of the pruritus. Thyroid-function studies can identify abnormal activity in
the thyroid gland, which may be manifested as pruritus.46
The erythrocyte sedimentation rate (ESR), although generally nonspecific, may be increased in autoimmune connective-tissue disorders or in infectious diseases, and it may be
extremely high in the presence of neoplastic disease.68

TREATMENT
General Measures
In the elderly, the management of pruritus poses a unique
challenge. Elderly patients with cognitive impairment may
make it impossible for them to identify a cause-and-effect
relationship between the pruritus and the routine activities of
daily living, or physical impairments may prevent them from
applying topical treatments.59 The management of pruritus in
this age group requires a patient-specific approach, in which
treatments are tailored to the patients mental and physical
disabilities, as well as to concurrent disease states, the severity of the pruritic symptoms, and the potential adverse effects
of available treatments.
Patient education is the first step in alleviating nonspecific
pruritic symptoms in elderly individuals. Patients should be
counseled to break the itchscratch cycle. Scratching can
cause increased cutaneous inflammation, thereby worsening
the itch.59 The cessation of scratching, therefore, may alleviate
the secondary irritation caused by the scratching itself. Moreover, patients should keep their nails short to avoid further
irritation of the skin if they are inclined to scratch.
Educating patients about the nonpharmacological measures that they can take to alleviate pruritic symptoms may
decrease the need for continuous pharmacological intervention. For example, patients should be instructed to take
short baths and to avoid hot water. Applying moisturizers immediately after bathing will ensure that the skin remains well
hydrated. Ideally, moisturizers with a low pH should be used
to maintain the normal acidic pH of the skin and to preserve
the skins barrier function.59 Using a twice-daily emollient,
especially one that contains 5% or 10% urea, may be beneficial,
although trial and error is often the method used to determine
which emollient works best.3
Patients should avoid alkaline cleansers and preparations
containing alcohol, as these tend to dry the skin. Mild, moisturizing bar soaps, such as Dove (Unilever), and soaps containing lanolin and glycerin are preferred over commercially
available pure soaps, such as Ivory (Procter & Gamble), because they cause less skin flaking after use.69
Wearing light, loose clothing while avoiding irritating fabrics,
such as wool, will also benefit the patient.70 To prevent excessive heat or perspiration, patients should maintain a comfortable air temperature in their homes, allowing less than 40%
moisture content.69 Using a humidifier in the winter and an air
conditioner in the summer is recommended.

Topical Therapies
Corticosteroids
Although corticosteroids are not directly antipruritic, they
are believed to produce their therapeutic effects by alleviating
the inflammation associated with some skin conditions, such

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as atopic dermatitis and psoriasis.70 Corticosteroids should
be used sparingly. Higher-potency steroid creams and ointments may provide an improved anti-inflammatory response,
but they also put the patient at increased risk for adverse effects, including skin atrophy, telangiectasia, and suppression
of the hypothalamuspituitary axis.70
Topical corticosteroids should be used with caution in the
elderly; these individuals may be particularly susceptible to the
skin-thinning effects of these drugs.70
Topical Immunomodulators
The topical calcineurin inhibitors tacrolimus (Protopic, Astellas) and pimecrolimus (Elidel, Novartis) are commonly used
in the treatment of atopic dermatitis. These agents are nonsteroidal selective inhibitors of the production and release of
inflammatory cytokines in T cells and of other pro-inflammatory mediators in mast cells.71
In a randomized trial comparing pimecrolimus cream 1%
with placebo in patients with atopic dermatitis, 56% of the
pimecrolimus group experienced a significant reduction in
the severity of pruritus compared with 34% of the placebo
group within 48 hours after treatment (P = 0.003).70
In another study, Stnder et al. evaluated the efficacy of
tacrolimus 0.1% and pimecrolimus 1% in patients with prurigo
nodularis (pruritic nodules of an unknown etiology) and in
patients with localized or generalized pruritus.72 Of the 20
patients who received these medications, eight (40%) achieved
a complete cessation of itching (a reduction of 70% to 90%).
Adverse drug effects included stinging and burning at the
application site.
If tolerated, topical immunomodulators might be a good
option for elderly patients with pruritus, because thinning and
atrophy of the skin are not a concern.
Coolants
Menthol and phenol are cyclic terpene alcohols that occur
naturally in plants. They affect delta-A nerve fibers, which
transmit the sensation of cold.73 The cooling sensation provided
by these agents may alleviate itching.
Although the optimal concentration of menthol has not been
established, products containing 1% menthol are commonly
used to relieve pruritus.74 With favorable safety and toxicity
profiles, menthol is a good option for relieving pruritus in
elderly patients.
Local Anesthetics
Agents that contain local anesthetics, such as lidocaine
(Lidoderm, Endo) and lidocaine/prilocaine (Emla, AstraZeneca), may relieve itching, especially when they are applied
with occlusive dressings of cloth or nylon.73
A local anesthetic made by Abbott, pramoxine HCl (also
known as pramocaine) has antipruritic properties and has
been used in hemodialysis patients with uremic pruritus.75
Prax Lotion (Ferndale) is another product that contains
pramoxine.
Polidocanol is a non-ionic surfactant with moisturizing and
local anesthetic properties, both of which help to ameliorate
pruritic symptoms. In an open-label study, polidocanol lotion
3%, when combined with urea 5%, significantly reduced pruritus

in patients with xerotic disorders, including atopic dermatitis,

contact dermatitis, and psoriasis.76
Capsaicin
As the main capsaicinoid in chili peppers, capsaicin exerts
its antipruritic effect by desensitizing sensory nerve fibers.77
It is beneficial in the treatment of neuropathic, systemic, and
dermatological pruritus. Adverse effects include pain, burning,
and stinging at the application site, which may cause patients
to stop treatment prematurely.
In a single-blind study involving healthy volunteers, the topical anesthetic cream EMLA (lidocaine 2.5%/prilocaine 2.5%)
was applied 60 minutes before capsaicin cream 0.075% was
applied on one forearm and before placebo was applied on the
other forearm.78 After 5 days of three-times-daily application,
pretreatment with Emla significantly reduced the burning
sensation from capsaicin, which may promote better adherence to capsaicin treatment.
Topical Cannabinoids
Cannabinoids act at peripheral sites and produce analgesia
through their actions on CB1 and CB2 receptors. The local
analgesic actions of agonists for CB2 receptors, such as
N-palmitoyl-ethanolamine (PEA), include the inhibition of
mast-cell function and inflammatory pain.79 PEA has been incorporated into topical analgesic preparations and has been
shown to reduce pruritus in patients with atopic dermatitis,
lichen simplex, and prurigo nodularis; it has also decreased
itching associated with chronic kidney disease.80,81
Topical Antihistamines
Topical antihistamines, such as diphenhydramine and pyrilamine, are used primarily to treat urticaria and insect bites.
These products are not usually used for other pruritic conditions, such as idiopathic local and generalized pruritus,
because of the side effects of erythema and skin irritation.73
Doxepin (Sinequan, Pfizer), a tricyclic antidepressant, exhibits potent histamine receptor (H1 and H2 ) antagonism. In a
double-blind study, Drake and Milikan compared the antipruritic efficacy and safety of doxepin HCl cream 5% (e.g.,
Prudoxin, Healthpoint) with a placebo vehicle in patients with
lichen simplex chronicus, nummular eczema, or contact
dermatitis.82 Twenty-four hours after initiation of treatment
and for the remainder of the 7-day study, almost all of the doxepin patients experienced significantly greater relief of pruritus compared with those receiving placebo (P < 0.002).
The most common side effects included a transient stinging
sensation after application (20.7%) and drowsiness (15.5%) resulting from systemic absorption. Although the drowsiness
subsided over time, this undesirable side effect may limit the
use of doxepin cream in elderly patients.
Topical Aspirin
A double-blind placebo-controlled study in patients with
lichen simplex chronicus (an intractable, itchy dermatosis)
demonstrated a significant improvement in the symptoms of
pruritus after treatment with an aspirin/dichloromethane solution.83 This option may be helpful for elderly patients who are
unable to tolerate long-term, high-potency steroids.
continued on page 236

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Pruritus in the Elderly

continued from page 232

Systemic Therapies
Antihistamines
Traditionally, the treatment of pruritus associated with various skin disorders has focused on medications that antagonize
histamine receptors. It has been proposed, however, that the
relief of itching achieved with these medications might be a
result of their sedating properties and not necessarily the
antagonism of histamine, especially in pruritic conditions such
as eczema, psoriasis, and lichen planus.84
Pruritus that results from the stimulation of histamine
receptors (as in urticaria) may be effectively treated with
antihistamines, such as diphenhydramine (Benadryl, McNeil
Consumer) because of their ability to antagonize histamine H1
receptors.13,75,84 The use of systemic antihistamines should be
avoided in elderly patients because of the anticholinergic
effects of these drugs.
Pruritus that is caused by the release of histamine is mediated by H1 receptors. Therefore, the nonsedating H2 receptor
antagonists, such as loratadine (Claritin, Schering-Plough)
and fexofenadine (Allegra, Sanofi), are generally not effective
in the treatment of histamine-related pruritus.13 These agents,
however, have favorable side-effect profiles, are relatively safe
in older persons, and may be an option for elderly patients with
pruritic dermatoses accompanied by erythema and wheals.13
Serotonin Receptor Antagonists
The antidepressant mirtazapine (Remeron, Organon), a
serotonin (5-HT2/5-HT3) receptor antagonist, is an effective
therapy for pruritus, particularly in patients with advanced
cancer, cholestasis, or hepatic or renal failure.85 The drugs
potential for causing drowsiness may be beneficial in patients
with nocturnal pruritus.86
In an open-label study, patients with chronic pruritus
received long-term treatment with the selective serotonin
reuptake inhibitors (SSRIs) paroxetine (e.g., Paxil, GlaxoSmithKline) and fluvoxamine (Luvox, Abbott).87 An antipruritic
effect was observed in 68% of the patients. Paroxetine and
fluvoxamine did not differ significantly in their efficacy. The
best responses occurred in patients with atopic dermatitis,
systemic lymphoma, or solid carcinoma.
Patients with cholestatic pruritus showed an antipruritic
response after they were treated with the antiemetic agent
ondansetron (Zofran, GlaxoSmithKline), a 5-HT3 receptor
antagonist.73
The use of serotonin receptor antagonists in elderly patients
may be limited by the occurrence of adverse effects, including
excessive CNS stimulation, sleep disturbances, and increased
agitation. It is important to consider the riskbenefit ratio of
these agents in the elderly; they should be administered only
as second-line or third-line therapy.3
Opioid Antagonists and Agonists
Opioid-induced pruritus occurs after activation of the muopioid receptors in the CNS. It is through this central process
that mu-opioid receptor antagonists, such as the generic drugs
naltrexone, nalmefene, and naloxone, are believed to have an
effect in treatment-resistant pruritus.88 These agents have
been used successfully to treat uremic and cholestatic pruritus, chronic urticaria, atopic dermatitis, prurigo nodularis,

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and opioid-induced pruritus.3,89

The activation of kappa-opioid receptors is known to reduce
pruritus. The kappa-opioid receptor agonists butorphanol (formerly Stadol, Apothecon) and nalfurafine (not available in the
U.S.) have been beneficial in patients with intractable itching
and uremic itching, respectively.59,90
Both opioid-receptor antagonists and agonists should be
used sparingly with supervision and caution in elderly patients.
These medications can put patients at risk for sedation and
insomnia, and they have a potential for abuse.
Neuroleptic Agents
The antiepileptic drugs gabapentin (Neurontin, Pfizer) and
pregabalin (Lyrica, Pfizer) decrease neuronal transmission.
Gabapentin is effective in the treatment of neurological pruritus (including brachioradial pruritus and notalgia paresthetica)
when used as a localized patch worn on the infrascapular area
of the back.91,92 Gabapentin is also effective in the treatment of
uremic pruritus.93
Because it is chemically similar to gabapentin, pregabalin
has been proposed as a therapy for chronic pruritus.94 Both
gabapentin and pregabalin are eliminated by the kidneys;
therefore, they must be administered appropriately in elderly
patients and in patients with impaired renal function to avoid
an overdose and adverse side effects.

Other Treatments
Phototherapy
Narrow-band ultraviolet-B (NBUVB) therapy is effective for
uremia-related pruritus and has achieved dramatic improvements in patients with severe itching.13 In a prospective study,
NBUVB was also effective in patients with generalized pruritus, although the therapys mechanism of action was not entirely clear.95 This approach may be a viable option, especially
in elderly patients, because the barrier of nonadherence to topical treatments does not come into play.
Psychotherapy
A meta-analysis was conducted to determine the effects of
psychological interventions in patients with atopic dermatitis.96
Eight clinical trials were reviewed, and numerous interventions
were evaluated, including aromatherapy, autogenic training,
brief dynamic psychotherapy, cognitivebehavioral therapy,
habit-reversal behavioral therapy, stress management, and
structured education. The investigators concluded that psychological interventions reduced the severity of eczema or the
intensity of itching and scratching in patients with atopic
dermatitis.
Acupuncture
Acupuncture interferes with the central and peripheral
transmission of itching through sensory nerve innervation,
which may be beneficial in patients with neuropathic pruritus,
prurigo nodularis, or uremic pruritus.97 Undertaking a review
of the literature, Carlsson et al. noted that pruritus had been
successfully treated with acupuncture in several trials, although the patient cohorts were small.97 Alternative modalities
may show promise for the treatment of pruritus in elderly
patients.

Pruritus in the Elderly

Treatment of Pruritus
Associated With Systemic Disease
Cholestatic Pruritus
Pruritus often develops in patients with hepatic disease. It
has been theorized that the accumulation of bile in nerve and
skin cells causes itching. Therapy in these patients should
focus on the underlying disease.38
The bile-acid sequestrants cholestyramine (e.g., Questran,
Par) and colestipol (Colestid, Pfizer) are used to treat cholestatic pruritus, and up to 80% of patients have shown a partial or
complete response to these drugs within 2 weeks.98 Because
cholestyramine and colestipol can interfere with the absorption
of many other drugs, they should not be administered within
4 hours before or after the use of certain agents. This schedule may be difficult for elderly patients who are taking multiple medications. Moreover, cholestyramine and colestipol are
associated with potentially significant gastrointestinal side effects, such as bloating, diarrhea, and abdominal discomfort.
Therefore, these drugs may need to be replaced with other
bile-acid sequestrants, such as colesevelam (Welchol, Daiichi
Sankyo).98
A double-blind, placebo-controlled study demonstrated the
efficacy and safety of naltrexone (ReVia, Duramed), an oral muopioid receptor antagonist, in cholestatic pruritus.99 Patients
with intrahepatic cholestasis who received naltrexone (50 mg)
showed a statistically significant improvement in daytime and
nighttime itching (P = 0.0003 and P = 0.001, respectively) compared with patients given placebo.
Several other treatments, including rifampin (Rifadin,
Sanofi), ursodeoxycholic acid (e.g., Actigall, Watson), propofol (Diprivan, AstraZeneca), phototherapy, SSRIs, and oral
cannabinoids, have also relieved cholestatic pruritus.98,100
Uremic Pruritus
The cause of uremic pruritus is not completely understood.
Treatment should be administered in a stepwise fashion using
drugs with favorable side-effect profiles. Optimizing dialysis
has been shown to improve pruritic symptoms in elderly
patients.100 Topical treatment with tacrolimus ointment (Protopic) reduces pruritus associated with chronic kidney disease
and may be a safe option in elderly patients.101
A randomized, double-blind, controlled comparative trial
was conducted to evaluate the benefits of an anti-itch lotion
containing 1% pramoxine in patients with moderate or severe
uremic pruritus who had received hemodialysis for at least
3 months.75 Fourteen patients were treated with the pramoxine-based lotion, and 14 were given a control lotion. The
pramoxine group experienced a significant reduction in the
intensity of itching (a 61% decrease) compared with controls
(a 12% decrease) (P = 0.0072).
In another study, gabapentin was effective in patients with
uremic pruritus who had undergone hemodialysis for more
than 3 months.93 The patients received gabapentin (100 mg)
after hemodialysis for 4 weeks. After a washout period of
1 week, they received placebo for another 4 weeks. On the
Visual Analogue Scale (VAS), mean pruritus scores were 6.44
(P < 0.0001), 15.00 (P < 0.001), and 81.11 (P < 0.001) during the
gabapentin, washout, and placebo periods, respectively.
Uremic pruritus has also been relieved with cholestyra-

mine, activated charcoal, thalidomide, oral opioid antagonists,

cannabinoids, capsaicin, phototherapy, pentoxifylline (Trental,
Sanofi), and acupuncture. 100,101
Hematological Malignancies
Pruritus that is directly associated with iron-deficiency
anemia responds to oral therapy with iron salts, and symptomatic improvement is seen within 14 days after treatment.100
Pruritus is also a key clinical feature of polycythemia vera.
Antihistamines, antidepressants, interferon-alpha, phlebotomy,
phototherapy, iron supplements, and myelosuppressive medications have had mixed results when used to treat the pruritus associated with this condition.102
Many other malignancies are associated with itching,
including Hodgkins lymphoma, myeloma, lymphoma, leukemia, paraproteinemia, Waldenstrms macroglobulinemia,
and mastocytosis. Pruritic patients with these malignancies
may experience relief after the underlying disorder has been
controlled.100
Many adults with HIV infection also have skin conditions,
including pruritus.103 Clinicians must keep this in mind when
treating elderly patients, and appropriate testing should be
done.

CONCLUSION
The ultimate determination of the cause of the common
complaint of pruritus remains a diagnostic dilemma and a
challenge for any physician. Identifying the cause of pruritus
in elderly patients with cognitive impairment can be even more
difficult. Every effort must be made to identify primary and
secondary causes of the disorder, and this can require excessive time and a meticulous history and physical examination.
Careful attention must be paid to even the slightest detail that
would lead the physician down the correct path.
When the cause has been determined, choosing the appropriate treatment is not always easy. The presence of comorbidities may make it difficult to select the correct treatment. In
elderly or other impaired persons, using therapies that require
a patients attention to drug schedules or other details is rife
with problems.
Physicians who treat patients with pruritus should consider
the adverse effects of all medications; be aware of patient complaints early in the process; and act in the patients best interest to improve quality of life and to eradicate discomfort.

REFERENCES
1. Yalcin B, Tamer E, Gur Toy G, et al. The prevalence of skin
diseases in the elderly: Analysis of 4099 geriatric patients. Int J
Dermatol 2006;45:672676.
2. Tycross R, Greaves MW, Handwerker H, et al. Itch: Scratching
more than the surface. Q J Med 2003;96:726.
3. Reich A, Stnder S, Szepietowski J. Pruritus in the elderly. Clin
Dermatol 2011;29:1523.
4. Fenske NA, Lober CW. Skin changes of aging: Pathological
implications. Geriatrics 1990;45:2735.
5. Wolkenstein P, Grob J, Bastuji-Garin S, et al. French people and
skin diseases. Arch Dermatol 2003;139:16141619.
6. Beauregard S, Gilchrest BA. A survey of skin problems and skin
care regimens in the elderly. Arch Dermatol 1987;123:16381643.
7. Dalgard F, Svenson A, Holm J, Sundby J. Self-reported skin morbidity in Oslo: Associations with sociodemographic factors among
adults in a cross-sectional study. Br J Dermatol 2004;151:452457.

Vol. 37 No. 4 April 2012

P&T 237

Pruritus in the Elderly

8. Kini S, DeLong L, Veledar E, et al. The impact of pruritus on quality of life: The skin equivalent of chronic pain. Arch Dermatol
2011;147(10):11531156.
9. Dalgard F, Dawn A, Yosipovich G. Are itch and chronic pain
associated in adults? Results of a large population survey in Norway. Dermatology 2007;214:305309.
10. Stnder S, Setinhoff M, Schmeltz M. Neurophysiology of pruritus. Arch Dermatol 2003;139:14631469.
11. Norman RA. Xerosis and pruritus in the elderly: Recognition and
management. Dermatol Ther 2003;16:254259.
12. Shanley KJ. Pathophysiology of pruritus. Vet Clin North Am Small
Anim Pract 1988;18:971981.
13. Tivoli Y, Rubenstin R. Pruritus: An updated look at an old problem. J Clin Anesth Dermatol 2009;2:3036.
14. Bernhard J. Itch and pruritus: What are they, and how should
itches be classified? Dermatol Ther 2005;18:288291.
15. Grundman S, Stnder S. Evaluation of chronic pruritus in older
patients. Aging Health 2010;6:5366.
16. Farange MA, Miller KW, Elsner P, Maibach H. Functional and
physiological characteristics of the aging skin. Aging Clin Exp Res
2008;20;195200.
17. Waller JM, Maibach HI. Age and skin structure and function, a
quantitative approach. I: Blood flow, pH, thickness, and ultrasound echogenicity. Skin Res Technol 2005;11:221235.
18. Waller JM, Maibach HI. Age and skin structure and function, a
quantitative approach. II: Protein, glycosaminoglycan, water and
lipid content, and structure. Skin Res Technol 2006;12:145154.
19. Stnder S, Weisshaar E, Luger T. Neurophysiological and neurochemical basis of modern pruritus treatment. Exp Dermatol
2007;17:161169.
20. Greaves MW, Wall PD. Pathophysiology of itching. Lancet 1996;
348:938940.
21. Rukweid R, Lischetzki G, McGlone F, et al. Mast cell mediators
other than histamine induce pruritus in atopic dermatitis patients:
A dermal microdialysis study. Br J Dermatol 2000;142:11141120.
22. Greaves MW, McDonald-Gibson W. Itch: Role of prostaglandins.
Br Med J 1973;3:608609.
23. Wallengren J. Neuroanatomy and neurophysiology of itch. Dermatol Ther 2005;18:292303.
24. Luger TA. Neuromediators: A crucial component of the skin
immune system. J Dermatol Sci 2002;30:8793.
25. Reamy B, Bunt C. A diagnostic approach to pruritus. Am Fam
Physician 2011;84:195202.
26. Rogers J, Harding C, Mayo A, et al. Stratum corneum lipids: The
effect of aging and the seasons. Arch Dermatol Res 1996;288:765
770.
27. Conti A, Rogers J, Verdejo P, et al. Seasonal influences on stratum
corneum ceramide 1 fatty acids and the influence of topical
essential fatty acids. Int J Cosmetic Sci 1996;18:112.
28. Hicks M, Elston D. Scabies. Dermatol Ther 2009;22:279292.
29. Hay RJ. Scabies and pyodermas: Diagnosis and treatment.
Dermatol Ther 2009;22:466474.
30. Ricci G, Dondi A, Patrizi A. Useful tools for the management of
atopic dermatitis. Am J Clin Dermatol 2009;10:287300.
31. Jinks SL, Carstens E. Superficial dorsal horn neurons identified
by intercutaneous histamine: Chemonociceptive responses and
modulation by morphine. J Neurophysiol 2000;84:616627.
32. Massey EW. Unilateral neurogenic pruritus following stroke.
Stroke 1984;15:901903.
33. Kimyal-Asadi A, Kimyal-Asadi T, Milani F. Post-stroke pruritus.
Stroke 1999;30:692693.
34. Lidell K. Post-herpetic pruritus (letter). Br Med J 1974;4:165.
35. Schneider G, Driesch G, Heuft G, et al. Psychosomatic cofactors
and psychiatric comorbidity in patients with chronic itch. Clin Exp
Dermatol 2006;31:762767.
36. Misery L, Alexandre S, Dutray S, et al. Functional itch disorder
or psychogenic pruritus: Suggested diagnosis criteria from the
French Psychodermatology Group. Acta Derm Venereol 2007;
87:341344.
37. Potts RO, Buras EM, Chrisman DA. Changes with age in the moisture content of human skin. J Invest Dermatol 1984;82:97100.
38. Mels M, Mancuso A, Burroughs AK. Pruritus in cholestatic and

238 P&T

April 2012 Vol. 37 No. 4

other liver diseases. Aliment Pharmacol Ther 2003;17:857870.

39. Oude E, Kremer AE, Martens JJ, Beuers UH. The molecular
mechanism of cholestatic pruritus. Digest Dis 2011;29:6671.
40. Oude E, Kermer E, Beuers U. Mediators of pruritus during
cholestasis. Curr Opin Gastroenterol 2011;27:289293.
41. Jones EA, Bergasa NV. The pruritus of cholestasis. Hepatology
1999;29:10031006.
42. Robinson-Bostom L, DiGiavanna J. Cutaneous manifestations of
end-stage renal disease. J Am Acad Dermatol 2000;43:975986.
43. Lugon J. Uremic pruritus: A review. Hemodial Int 2005;9:180188.
44. Peharda V, Gruber F, Kastelan M, et al. Pruritus: An important
symptom of internal diseases. Acta Dermatovenerol Alp Panonica
Adriat 2000;9:114.
45. Yamaoka H, Sasaki H, Yamasaki H, et al. Truncal pruritus of
unknown origin may be a symptom of diabetic polyneuropathy.
Diabetes Care 2010;33:150155.
46. Artantas S, Gul U, Kilic A, Guler S. Skin findings in thyroid diseases. Eur J Intern Med 2009;20;158161.
47. Karnath B. Pruritus: A sign of underlying disease. Hosp Physician
2005 (October); 2529.
48. Hasan M, Tierney W, Baker, M. Severe cholestatic jaundice in
hyperthyroidism after treatment with 131-iodine. Am J Med Sci
2004;328:348350.
49. Polat M, Oztas P, Ilhan M, et al. Generalized pruritus: A prospective study concerning etiology. Am J Clin Dermatol 2008;9:3944.
50. Callen J, Bernardi D, Clark R, Weber D. Adult-onset recalcitrant
eczema: A marker of noncutaneous lymphoma or leukemia. J Am
Acad Dermatol 2000;43(2 Pt 1):207210.
51. Fitzsimmons E, Dagg J, McAllister EJ. Pruritus of polycythaemia
vera: A place for pizotifen? Br Med J (Clin Res Ed)1981;283:277.
52. Steckelings UM, Artuc M, Wollschager T, et al. Angiotensinconverting enzyme inhibitors as inducers of adverse cutaneous
reactions. Acta Derm Venereol 2001;81:321325.
53. Van der Linden PD, Van Der Lei J, Vlug AE, Stricker BH. Skin
reactions to antibacterial agents in general practice. J Clin Epidemiol 1998;51:703708.
54. Reich A, Stnder S, Szepietowski J. Drug-induced pruritus:
A review. Acta Derm Venereol 2009;89:236244.
55. Daras RH, Kashyap ML, Knopp RH, et al. Long-term safety and
efficacy of a combination of niacin extended release and simvastatin in patients with dyslipidemia: The OCEANS study. Am J
Cardiovasc Drugs 2008;8:6981.
56. Nigen S, Knowles SR, Shear NH. Drug eruptions: Approaching
the diagnosis of drug-induced skin diseases. J Drugs Dermatol
2003;2:278299.
57. Swegle JM, Logemann C. Management of common opioidinduced adverse effects. Am Fam Physician 2006;74:13471354.
58. Valeyrie-Allanore L, Sassolas B, Roujeau J. Drug-induced skin,
nail, and hair disorders. Drug Saf 2007;30:10111030.
59. Patel T, Yosipovich G. The management of chronic pruritus in the
elderly. Skin Ther Lett 2010;15:59.
60. Farage MA, Miller KW, Berardesca E, Maibach HI. Clinical implications of aging skin. Am J Clin Dermatol 2009;10:7386.
61. Stnder S, Weisshaar E, Mettang T, et al. Clinical classification of
itch: A position paper of the International Forum for the Study of
Itch. Acta Derm Venereol 2007;87:291294.
62. Cassano N, Tessari G, Vena G, Girolomoni G. Chronic pruritus
in the absence of specific skin disease. Am J Clin Dermatol 2010;
11:399411.
63. Greco PJ, Ende J. Pruritus: A practical approach. J Gen Intern Med
1992;7:340349.
64. Savin JA. Diseases of the skin: The management of pruritus.
Br Med J 1973;4:779780.
65. Keehn C, Morgan M. Clinicopathologic attributes of common
geriatric dermatologic entities. Dermatol Clin 2004;22:115123.
66. Moses S. Pruritus. Am Fam Physician 2003;68:11351142.
67. Lonsdale-Eccles A, Carmichael AJ. Treatment of pruritus associated with systemic disorders in the elderly. Drugs Aging 2003;
20:198208.
68. Hiramanek N. Itch: A symptom of occult disease. Aust Fam Physician 2004;33:495499.
69. Boccanfuso SM, Cosmet L, Volpe AR, et al. Skin xerosis: Clinical

Pruritus in the Elderly

70.
71.
72.
73.
74.
75.

76.
77.
78.
79.
80.

81.

82.
83.
84.
85.
86.
87.

88.
89.
90.
91.
92.
93.
94.

report on the effect of a moisturizing bar soap. Cutis 1978;21:703

707.
Patel T, Yosipovich G. Therapy of pruritus. Exp Opin Pharmacother
2010;10:16731682.
Kaufman R, Bieber T, Helgesen AL, et al. Onset of pruritus relief
with pimecrolimus cream 1% in adult patients with atopic dermatitis: A randomized trial. Allergy 2006:61:375381.
Stnder A, Shurmeyer-Horst F, Luger TA, et al. Treatment of
pruritic diseases with topical calcineurin inhibitors. Ther Clin
Risk Manage 2006;2:213218.
Yosipovitch G, David M. The diagnostic and therapeutic approach
to idiopathic generalized pruritus. Int J Dermatol 1999;38:881887.
Patel T, Ishiuji Y, Yosipovitch G. Menthol: A refreshing look at this
ancient compound. J Am Acad Dermatol 2007;57:873878.
Young TA, Patel TS, Camacho F, et al. A pramoxine-based anti-itch
lotion is more effective than a control lotion for the treatment of
uremic pruritus in adult hemodialysis patients. J Dermatol Treat
2009;20:7681.
Freitag G, Hoppner T. Results of a postmarketing drug-monitoring survey with a polidocanolurea preparation for dry, itching
skin. Curr Med Res Opin 1997;13:529537.
Papoiu AD, Yosipovitch G. Topical capsaicin: The fire of a hot
medicine is reignited. Exp Opin Pharmacother 2010;11:1359
1371.
Yosipovitch G, Maibach HI, Rowbotham MC. Effect of EMLA
pre-treatment on capsaicin-induced burning and hyperalgesia.
Acta Derm Venereol 1999;79:118121.
Jorge LL, Feres CC, Teles VE. Topical preparations for pain relief:
Efficacy and patient adherence. J Pain Res 2010;20:1124.
Szepietowski JC, Szepieowski T, Reich A. Efficacy and tolerance
of the cream containing structured physiological lipids with
endocannabinoids in the treatment of uremic pruritus: A preliminary study. Acta Dermatovenerol Croat 2005;13:97103.
Eberlein B, Eicke C, Reinhardt HW, et al. Adjuvant treatment of
atopic eczema: Assessment of an emollient containing N-palmitoylethanolamine (ATOPA study). J Eur Acad Dermatol Venereol
2008;22:7382.
Drake LA, Milikan LE. The antipruritic effect of 5% doxepin cream
in patients with eczematous dermatitis. Arch Dermatol 1995;
131:14031408.
Yosipovitch G, Sugeng, MW, Chan YH, et al. The effect of topically
applied aspirin on localized circumscribed neurodermatitis.
J Am Acad Dermatol 2001;45:910913.
Krause L, Shuster S. Mechanism of action of antipruritic drugs.
Br Med J (Clin Res Ed) 1983;287:11991200.
Davis MP, Frandsen JL, Walsh D, et al. Mirtazepine for pruritus.
J Pain Symptom Manage 2003;25:288291.
Hundley JL, Yosipovitch G. Mirtazepine for reducing nocturnal
itch in patients with chronic pruritus: A pilot study. J Acad Dermatol 2006;55:543544.
Stnder S, Bockenholt B, Schurmeyer-Horst F, et al. Treatment
of chronic pruritus with the selective serotonin re-uptake
inhibitors paroxetine and fluvoxamine: Results of an open-labelled,
two-arm proof-of-concept study. Acta Derm Venereol 2009;89:
4551.
Reich A, Scepietowski JC. Opioid-induced pruritus: An update.
Clin Exp Dermatol 2010; 35:26.
Phan NJ, Bernhard JD, Luger TA, et al. Antipruritic treatment with
systemic mu-opioid receptor antagonists: A review. J Am Acad
Dermatol 2010;63:680688.
Dawn AG, Yosipovitch G. Butorphanol for treatment of intractable
pruritus. J Am Acad Dermatol 2006;54:527531.
Yesudian PD, Wilson NJ. Efficacy of gabapentin in the management of pruritus of unknown origin. Arch Dermatol 2005;141:
15071509.
Loosemore MP, Bordeaux JS, Bernhard JD. Gabapentin treatment
for notalgia paresthetica, a common isolated peripheral sensory
neuropathy. J Eur Acad Dermatol Venereol 2007;21:14401441.
Razhegi E, Eskandari D, Ganji MR, et al. Gabapentin and uremic
pruritus in hemodialysis patients. Renal Fail 2009;31:8590.
Ehrchen J, Stnder S. Pregabalin in the treatment of chronic
pruritus. J Am Acad Dermatol 2008;58:S36S37.

95. Seckin DS, Demircay Z, Akin O. Generalized pruritus treated with

narrow-band UVB. Int J Dermatol 2007;46:367370.
96. Chida Y, Steptoe A, Hirakawa N, et al. The effects of psychological intervention on atopic dermatitis: A systematic review and
meta-analysis. Int Arch Allergy Immunol 2007;144:19.
97. Carlsson CP, Wallengren J. Therapeutic and experimental therapeutic studies on acupuncture and itch: Review of the literature.
J Eur Acad Dermatol Venereol 2010;24:10131016.
98. Kremer AE, Beuers U, Oude-Elferink RPJ. Pathogenesis and
treatment of pruritus in cholestasis. Drugs 2008;68:21632182.
99. Terg R, Coronel E, Sorda J, et al. Efficacy and safety of oral
naltrexone treatment for pruritus of cholestasis: A crossover,
double blind, placebo-controlled study. J Hepatol 2002;37:717
722.
100. Lonsdale-Eccles A, Carmichael AJ. Treatment of pruritus associated with systemic disorders in the elderly: A review of the role
of new therapies. Drugs Aging 2003;20:197208.
101. Mettang T, Weisshaar E. Pruritus: Control of itch in patients
undergoing dialysis. Skin Ther Lett 2010;15:15.
102. Saini KS, Patnaik MM, Tefferi A. Polycythemia vera-associated
pruritus and its management. Eur J Clin Invest 2010;40:828834.
103. Serling SL, Leslie K, Maurer T. Approach to pruritus in the adult
HIV-positive patient. Semin Cutan Med Surg 2011;30:101106. I

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